In vitro interference of tigecycline at subinhibitory concentrations on biofilm development by Enterococcus faecalis

Maestre, Juan Ramón; Aguilar, Lorenzo; Mateo, María; Giménez, María-José; Méndez, M.L.; Alou, Luís; Granizo, Juan-José; Prieto, J.

doi:10.1093/jac/dks014

Cited by 24 publications

(16 citation statements)

References 7 publications

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“…Tigecycline has previously been reported to inhibit biofilm formation in enterococci. Maestre and colleagues demonstrated that tigecycline decreased the adherence of 55% of the isolates that had strong biofilm-formation ability 39 . To the best of our knowledge, there are no published reports of biofilm inhibition by vancomycin in enterococci, but there is a precedent case reported for a clinical staphylococcal isolates 16 .…”

Section: Discussionmentioning

confidence: 99%

Biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin

Hashem

Amin

Essam

et al. 2017

Sci Rep

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Enterococci are nosocomial pathogens that can form biofilms, which contribute to their virulence and antibiotic resistance. Although many genes involved in biofilm formation have been defined, their distribution among enterococci has not been comprehensively studied on a genome scale, and their diagnostic ability to predict biofilm phenotypes is not fully established. Here, we assessed the biofilm-forming ability of 90 enterococcal clinical isolates. Major patterns of virulence gene distribution in enterococcal genomes were identified, and the differentiating virulence genes were screened by polymerase chain reaction (PCR) in 31 of the clinical isolates. We found that detection of gelE in Enterococcus faecalis is not sufficient to predict gelatinase activity unless fsrAB, or fsrB alone, is PCR-positive (P = 0.0026 and 0.0012, respectively). We also found that agg is significantly enriched in isolates with medium and strong biofilm formation ability (P = 0.0026). Additionally, vancomycin, applied at sub minimal inhibitory concentrations, inhibited biofilm in four out of five strong biofilm-forming isolates. In conclusion, we suggest using agg and fsrB genes, together with the previously established gelE, for better prediction of biofilm strength and gelatinase activity, respectively. Future studies should explore the mechanism of biofilm inhibition by vancomycin and its possible use for antivirulence therapy.

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Section: Discussionmentioning

confidence: 99%

Biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin

Hashem

Amin

Essam

et al. 2017

Sci Rep

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“…The selected microorganisms are responsible for >95% of infections related with permanent devices used in clinical practices. All strains were purchased from American Type Culture Collection and were strong biofilm producers as determined spectrophotometrically by the crystal violet staining method [26,27] on polystyrene flat-bottom 96-well microtiter plates (Greiner bio-one, Kremsmünster, Austria) (data not shown).…”

Section: Methodsmentioning

confidence: 99%

Effect of the Medium Composition on the Zn2+ Lixiviation and the Antifouling Properties of a Glass with a High ZnO Content

et al. 2017

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The dissolution of an antimicrobial ZnO-glass in the form of powder and in the form of sintered pellets were studied in water, artificial seawater, biological complex media such as common bacterial/yeast growth media (Luria Bertani (LB), yeast extract, tryptone), and human serum. It has been established that the media containing amino acids and proteins produce a high lixiviation of Zn2+ from the glass due to the ability of zinc and zinc oxide to react with amino acids and proteins to form complex organic compounds. The process of Zn2+ lixiviation from the glass network has been studied by X-ray photoelectron spectroscopy (XPS). From these results we can state that the process of lixiviation of Zn2+ from the glass network is similar to the one observed in sodalime glasses, where Na+ is lixiviated to the media first and the fraction of Zn that acts as modifiers (~2/3) is lixiviated in second place. After the subsequent collapse of the outer surface glass layer (about 200–300 nm thick layer) the dissolution process starts again. Antifouling properties against different bacteria (S. epidermidis, S. aureus, P. aeruginosa, E. coli, and M. lutea) have also been established for the glass pellets.

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“…Subinhibitory antibiotic concentrations have been shown to affect the physioelectrical (34) and adhesion (35) behavior of E. faecalis. In addition, low concentrations of tigecycline have been shown to reduce biofilm formation even when the growth of planktonic cells is not significantly affected (36). To our knowledge, however, this is the first work to describe enhancement of biofilm formation by E. faecalis due to cell wall synthesis inhibitors.…”

Section: Discussionmentioning

confidence: 85%

Interplay between antibiotic efficacy and drug-induced lysis underlies enhanced biofilm formation at subinhibitory drug concentrations

Hallinen

Wood

2017

Preprint

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Subinhibitory concentrations of antibiotics have been shown to enhance biofilm formation in multiple bacterial species. While antibiotic exposure has been associated with modulated expression of many biofilm-related genes, the mechanisms of drug-induced biofilm formation remain a focus of ongoing research efforts and may vary significantly across species. In this work, we investigate antibiotic-induced biofilm formation in Enterococcus faecalis, a leading cause of nosocomial infections. We show that biofilm formation is enhanced by subinhibitory concentrations of cell wall synthesis inhibitors but not by inhibitors of protein, DNA, folic acid, or RNA synthesis. Furthermore, enhanced biofilm is associated with increased cell lysis, increases in extracellular DNA (eDNA) levels, and increases in the density of living cells in the biofilm. In addition, we observe similar enhancement of biofilm formation when cells are treated with nonantibiotic surfactants that induce cell lysis. These findings suggest that antibiotic-induced biofilm formation is governed by a trade-off between drug toxicity and the beneficial effects of cell lysis. To understand this trade-off, we developed a simple mathematical model that predicts changes in antibiotic-induced biofilm formation due to external perturbations, and we verified these predictions experimentally. Specifically, we demonstrate that perturbations that reduce eDNA (DNase treatment) or decrease the number of living cells in the planktonic phase (a second antibiotic) decrease biofilm induction, while chemical inhibitors of cell lysis increase relative biofilm induction and shift the peak to higher antibiotic concentrations. Overall, our results offer experimental evidence linking cell wall synthesis inhibitors, cell lysis, increased eDNA levels, and biofilm formation in E. faecalis while also providing a predictive quantitative model that sheds light on the interplay between cell lysis and antibiotic efficacy in developing biofilms.KEYWORDS Enterococcus, biofilms, mathematical modeling, subinhibitory antibiotics B iofilms are dense, surface-associated, microbial communities that play important roles in infectious diseases and a range of device-related clinical infections (1, 2). Biofilms exhibit a fascinating range of community behavior (3), including long-range metabolic codependence (4) and electrical signaling (5-7), phenotypic phase variation (8) and spatial heterogeneity (9), strong ecological competition (10), and multiple types of cooperative behavior, including collective resistance to antimicrobial therapy (11-13). The biofilm response to antibiotics has been a topic of particular interest, with biofilms across species showing dramatically increased resistance to antibiotics relative to planktonic cells. However, a number of studies have shown, somewhat counterintuitively, that exposure to sublethal doses of antibiotics may enhance biofilm formation in a wide range of species (14-16). While antibiotic-mediated biofilm induction has been associated with modul...

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In vitro interference of tigecycline at subinhibitory concentrations on biofilm development by Enterococcus faecalis

Abstract: In vitro tigecycline subinhibitory concentrations were able to interfere with biofilm formation by E. faecalis.

Cited by 24 publications

References 7 publications

Biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin

Biofilm formation in enterococci: genotype-phenotype correlations and inhibition by vancomycin

Effect of the Medium Composition on the Zn2+ Lixiviation and the Antifouling Properties of a Glass with a High ZnO Content

Interplay between antibiotic efficacy and drug-induced lysis underlies enhanced biofilm formation at subinhibitory drug concentrations

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